Journal
NATURE IMMUNOLOGY
Volume 15, Issue 10, Pages 957-U201Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2985
Keywords
-
Categories
Funding
- National Institute of Allergy and Infectious Diseases [AI061061]
- American Cancer Society [RSG-09-045-01-DDC]
Ask authors/readers for more resources
Despite the increasing knowledge of the molecular events that induce the glycolysis pathway in effector T cells, very little is known about the transcriptional mechanisms that dampen the glycolysis program in quiescent cell populations such as memory T cells. Here we found that the transcription factor Bcl-6 directly repressed genes encoding molecules involved in the glycolysis pathway, including Slc2a1, Slc2a3, Pkm and Hk2, in type 1 helper T cells (T(H)1 cells) exposed to low concentrations of interleukin 2 (IL-2). Thus, Bcl-6 had a role opposing the IL-2-sensitive glycolytic transcriptional program that the transcription factors c-Myc and HIF-1 alpha promote in effector T cells. Additionally, the T(H)1 lineage-specifying factor T-bet functionally antagonized the Bcl-6-dependent repression of genes encoding molecules in the glycolysis pathway, which links the molecular balance of these two factors to regulation of the metabolic gene program.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available